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module 103 - theme 2 > thrombotic disorders > Flashcards

thrombotic disorders Flashcards

1
Q

what are thrombotic risk factors?

A
  • post operative (especially orthopaedic)
  • hospitalisation
  • cancer
  • pregnancy
  • OCP
  • long-haul flights
  • obesity
  • IV drug use
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2
Q

what presents when you have deep vein thrombosis?

A
  • can be no symptoms at all
  • unilateral calf swelling/heat/pain/redness/hardness
  • differential diagnosis: cellulitis, Bakers’ cyst, muscular pain
  • potentially fatal if missed
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3
Q

what is a doppler ultrasound?

A

transducer produces real-time two dimensional image of soft tissue structure

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4
Q

what shows velocity and direction of blood flow?

A

colour duplex

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5
Q

what is Doppler ultrasound used for?

A
  • veins are non-compressible by U/S probe
  • investigation of choice
  • venogram done in past
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6
Q

what is the D-dimer test?

A

a test that assesses the likelihood of having a deep vein thrombosis

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7
Q

what do D-dimers do?

A

indicate activation of the clotting cascade

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8
Q

what do the results of a D-dimer show?

A
  • low wells score and negative D-dimer test have a high negative predictive value
  • high wells score or positive D-dimer then proceed to U/S scan to confirm DVT
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9
Q

what is the initial treatment of a deep vein thrombosis?

A
  • therapeutic anti-coagulation using sub-cut LMW heparin (such as tinzaparin or enoxaparin)
  • dose of LMW heparin according to patients weight
  • no monitoring required (can use anti-Xa assay)
  • ensure adequate EGFR >30ml/min
  • otherwise use iv unfractionated heparin
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10
Q

what do you do when you have your first deep vein thrombosis?

A

anti-coagulated for 6 months

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11
Q

what do you do when you have your second deep vein thrombosis

A

lifelong anticoagulation

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12
Q

what is a PE?

A

pulmonary embolus

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13
Q

what are the symptoms of a PE?

A
  • pleuritic pain
  • dyspnoea
  • haemoptysis
  • syncope
  • death
  • tachycardia
  • tachypnoea
  • hypotension
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14
Q

what is a V/Q san?

A

ventilation/perfusion radio-isotope scan

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15
Q

what does under-perfusion lead to?

A

V/Q mismatch

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16
Q

what is the limitation of a V/Q scan?

A

underlying disease

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17
Q

what shows on an ECG when you have deep vein thrombosis?

A
  • sinus tachycardia
  • atrial fibrillation
  • right heart strain (RBBB)
  • classic: SI, QIII, TIII (rare)
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18
Q

what are the PE outcomes?

A
  • 5% mortality rate despite treatment
  • 4% develop pulmonary hypertension
  • cause of death in 10-30% of in-patient post-mortems
  • up to 60% have micro-emboli at post-mortem
  • a leading cause of preventable death in the western world
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19
Q

how do you treat a massive PE?

A
  • Mx: thrombolysis with tPA (alteplase), tissue plasminogen activator
  • iv unfractionated heparin (monitor with APTR)
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20
Q

how do you treat a standard PE?

A
  • LMW heparin injections
  • warfarin for 6 months
  • consider underlying causes
  • LMW heparin is better if underlying cancer
  • IVC filters
  • consider a DOAC as an alternative (dabigatran po, rivaroxaban po)
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21
Q

what are inherited causes of thrombophilia screen?

A
  • factor V leiden

- deficiency of natural anticoagulants (anti-thrombin deficiency, protein c deficiency, protein s deficiency)

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22
Q

what are the acquired causes of thrombophilia?

A
  • anti-phospholipid syndrome

- test for lupus anticoagulant (DRVVT) and anticardiolipin Abs

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23
Q

what are examples of anti-thrombotics?

A
  • warfarin
  • heparin
  • newer agens
  • anti-platelets drugs
  • fibrinolytic agents
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24
Q

what is warfarin?

A

a vitamin K antagonist that prevents gamma- carboxylation of factors II, VII, IX, X

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25
Q

what prolongs the extrinsic pathway?

A

warfarin

26
Q

what monitors warfarin?

A

international normalised ratio

27
Q

what is the international normalised ratio for warfarin?

A

2.5 for DVT, PE and AF and 3.5 for recurrent VTE or metal heart valves

28
Q

what are the half-lives for the different clotting factor?

A

VII - 6 hours
IX - 24 hours
X - 40 hours
II - 60 hours

29
Q

what natural anti-coagulants does warfarin inhibit?

A
  • protein c

- protein s

30
Q

what inhibits and induces warfarin?

A
  • enzyme inhibitors potentiate warfarin

- enzyme inducers inhibit warfarin

31
Q

how does alcohol interact with warfarin?

A
  • binge drinking tends to potentiate warfarin

- chronic alcoholism tends to inhibit warfarin

32
Q

what is warfarin control affected by?

A
  • binding to albumin
  • absorption of vitamin k from GI tract
  • synthesis of vitamin k factor by liver
  • hereditary resistance
33
Q

what are the side-effects of warfarin?

A
  • teratogenic
  • significant haemorrhage risk
  • minor bleeding up to 20% per year
  • skin necrosis
  • alopecia
34
Q

how do you reverse warfarin?

A

in life-threatening bleeds you give activated prothrombin complex which contains vitamin k dependent factors II, VII, IX and X

35
Q

what does do you give activated prothrombin in?

A

25-50 units per kg depending on INR level

36
Q

what other treatments can you give to reverse warfarin?

A
  • give vitamin K 2-10mg depending on INR level

- fresh frozen plasma (FFP) but it is not optimised for warfarin reversal

37
Q

what is heparin?

A

mucopolysaccharide that works by potentiating anti-thrombin

38
Q

what does heparin do?

A

irreversibly inactivates factor IIa and factor Xa

39
Q

how is heparin administered?

A

by an injection

40
Q

what are the 2 formulations of heparin?

A
  • unfactionated heparin given by iv infusion

- low molecular weight heparin given sc injections

41
Q

how is unfactionated heparin given?

A

iv with 5000U bolus and ~1000U/hour infusion

42
Q

what is unfactionated heparin safe for?

A

renal failure as it is metabolised by the liver and not renally excreted

43
Q

what is a rare complication or heparin?

A

heparin-induced thrombocytopenia

44
Q

why is low molecular weight heparin convenient?

A

due to once daily sc injections and prescribed due to the patient’s weight

45
Q

what must a patient have before being prescribed low molecular weight heparin?

A

creatine clearance of over 30ml/minute

46
Q

what were direct oral anti-coagulants developed as?

A

oral alternatives to warfarin

47
Q

what are benefits to direct oral anti-coagulants?

A

no monitoring required, flat dosing, good safety profile

48
Q

what are the 2 classes of direct oral anti-coagulants?

A
  • direct thrombin inhibitor

- direct factor Xa inhibitor

49
Q

what is Rivaroxaban?

A

a direct factor Xa inhibitor which causes irreversible anti-coagulation

50
Q

what are the signs that indicate you need to use Rivaroxaban?

A
  • VTE prophylaxis
  • used for treatment of DVTs and PEs
  • stroke prevention in atrial fibrillation
51
Q

what is an alternative to rivaroxaban?

A

apixaban

52
Q

what is dabigatran?

A

a direct thrombin inhibitor

53
Q

what are the signs that indicate you need to use dabigatran?

A
  • VTE prophylaxis
  • used for treatment of DVTs and PEs
  • stroke prevention in arial fibrillation
54
Q

what reverses dabigatran?

A

Praxbind

55
Q

what are different types of anti-platelet drugs?

A
  • aspirin (cyclo-oxygenase inhibitor)
  • clopidogrel (ADP receptor blocker)
  • dupyridamole (inhibits phosphodiesterase)
  • prostacyclin (stimulates adenylate cyclase)
  • glycoprotein IIb/IIIa inhibitors
56
Q

what procedure are anti-platelet drugs used in?

A

angioplasty procedures

57
Q

what are fibrinolytic agents?

A

thrombotic agents used to lyse fresh thrombi by converting plasminogen to plasmin

58
Q

what are examples of fibrinolytic agents?

A
  • tissue plasminogen activator (tPA, Alteplase)
  • streptokinase
  • urokinase
59
Q

when are fibrinolytic agents administered?

A

systemically in actute MI, recent thrombotic stroke, major PE or massive iliofemoral thrombosis

60
Q

what are the risks/things you need to be aware of with fibrinolytic agents?

A
  • beware of contra-indicators to thrombolysis

- risk-benefit ratio = haemorrhage/thrombotic risk balance

module 103 - theme 2 (8 decks)

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